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K                                                         K 
#(-27<                                         PREVENTION AND MANAGEMENT                           OF PRESSURE SORES                       EDWARD J. MATHES, RPA-C                            Hahnemann University                      Physician Assistant Program                         Philadelphia, PA 19102                                    and                            The Genesee Hospital                         Department of Surgery                          224 Alexander Street                          Rochester, NY 14607                  Written Comments invited at The Genesee Hospital Address                            Abbreviated Title:  pressure sores                                                ABSTRACT      Pressure sores are a vexing problem estimated to affect 3-25% of all patients in acute and long-term care facilities.  Entrinsic factorsthat favor pressure sore development include pressure, shear, friction, and moisture.  There are multiple intrinsic contributors.  Frevention is preferable to treatment.  Using available tools, patients at-risk for developing pressure sores can be identified and preventive measures instituted.  When prevention fails, treatment,based on 5 therapeutic principles, will facilitate healing.                                 EPIDEMIOLOGY        Pressure ulcers (sores) are an unfortunate problem that carry significant morbidity and mortality. Three distinct groups of patients are affected: spinal-cord injured, geriatric, and orthopedic [1,2,3]. The National Pressure Ulcer Advisory Panel, at their 1988 meeting, reported an incidence of 3% - 14% among all patients in acute care institutions [4,5], rising to 15% - 25% if long-term care patients are included [6].  Additionally, all patients who have or develop pressure sores are hospitalized an average of five times longer, experience a five-fold increase in mortality, and cost an average of $35,000.00 more, per patient, when compared to the general patient populations[5,6,7,8].                                    ETIOLOGY        There are 4 primary extrinsic factors associated with pressure sore development:  pressure, shear, fricion, and moisture.   1).  Pressure: Most pressure sores occur in those areas where soft tissue is compressed between bony prominences and a firm surface (focal pressure).  80% occur on the lower body; the sacral-coccygeal area, the greater trochanters, ischial tuberosities, malleoli, and heels being most commonly affected [8].  Other sites include the elbows, occiput,scapulae and spinus processes.  External, focal pressure that exceeds capillary filling pressure (32 mmHg) for as little as two hours can cause ischemic change# [9,10].  As pressure is increased, ischemia occurrs over a progressively shorter time [11]. Additionally, deeper tissues appear tobe more suceptible than skin to ischemia [12,13].  2).  Shear occurs when adjacent tissue surfaces (skin & fascia) slide, creating a relative displacement of tissues, causing acute angulation and stretch of blood vessels and lymphatics, resulting in decreasedperfusion, ischemia, and dermal undermining [14,15].  3).  Friction occurs when two surfaces are moved across one another. Friction disrupts the protective outer layers of the skin, interfering with the fibrinolytic activity of the dermis, making the skin moresuseptible to pressure necrosis [15].  4).  Moisture due to fecal and urinary incontinence causes tissue maceration, accelerates skin breakdown, and increases the friction co-efficient.      There are a variety of intrinsic factors that contribute to pressure sore formation.  Neurologic diseases that cause sensory deficits rob the patient of the ability to sense the pain associated with local tissue ischemia.  Immobility due to over-sedation, contractures, fractures, spinal cord injury, and other causes interfere with the patient's ability to change positions when pressure tolerances are exceeded [16,17]. The loss of protective fat padding over bony prominences occurs with weight loss.  Large and small vessel vascular disease interferes with tissue perfusion.  skin changes associated with age (inelasticity, transparency, etc), hypoalbuminemia, andmalnutrition have also been implicated [5,18,19,20].                                  PREVENTION        Because of the financial, physical, and emotional morbidity associated with pressure sores, prevention is preferable to treatment. A simple program, stressing the total elimination of risk factors, isusually the best.      Nursing experts have developed many tools to help identify patients at risk for pressure sore formation [21,22]. Most use a scoring system that assigns a numeric value to selected risk factors.Higher scores usually indicate greater risk.                             PREVENTIVE MEASURES        Once identified as `at-risk', prevention of skin breakdown is of prime importance.  Underlying disease should be treated and/or controlled, patients' skin should be inspected at regular intervals, preferably daily, nutritional status assessed, and malnutritiontreated.      Pressure Relief is effected by interposing soft material between the, mattress and bony prominences frequent turning [23].  The goal is to reduce pressure on the usual pressure ulcer sites below capillaryfilling pressure (32mmHg).      There are many mattress overlays and total bed systems available. All have their advantages, disadvantages, and levels of effectiveness [24]. A complete discussion is beyond the scope of this paper.However, a brief description of a few types is presented.      Convoluted Foam or eggcrate mattress overlays are relatively inexpensive, easy to use, and may improve patient comfort.  Their efficacy at preventing pressure ulcers is questionable as most do notreduce focal pressure significantly.      Air matresses come in many shapes and forms, including static yair, alternating air-pressure, and low-air-loss systems.  Static air mattresses are comparable to foam overlays.  Alternating pressure air mattresses consist of a pump and multiple, interconnected cells that alternately inflate and deflate to relieve pressure.  Low-air-loss beds (Mediscus(R) & others) consist of multiple, individual, layered air cells.  Pressure in each individual cell can be varied according to theneeds of the patient.      Air Fluidized Beds (Clinitron(R) & others) consist of silicone microspheres encased in an air and liquid permeable cover.  Warm air is circulated in the cover, allowing the patient to "float" on a fluid-like surface with less than l0mmHg pressure exerted [25].      Your selection of an appropriate system should be based on it's ability to protect patients at different levels of risk.  Foam (eggcrate) overlays may be adequate for "low risk" patients, the air-fluidized bed reserved for those at higher risk [26].        FRlCTION is prevented by using lotion as a skin lubricant, lifting (not dragging) the patient across the bed, and ensuring bedcloths arewrinkle free.        SHEAR is prevented by keeping the head of the bed lower than 30degrees.        IMMOBILE patients should be turned every two hours to relieve pressure.  The 30 degree right and left lateral oblique positions will relieve pressure on all bony prominences [23]. If the patient's condition permits, range of motion exercises and ambulationshould beincorporated into the prevention regimen.        lNCONTlNENCE is a major source of moisture and bacterial contamination.  Urinary incontinence can be contained with external collection devices.  lndwelling bladder catheters work well, but serveas a portal for bacterial entry.      Bowel incontinence is more difficult to control.  External fecal collection devices are available and, reportedly, easy to use.  Rectal tubes, if improperly used, run the risk of anal stenosis, fistula formation, or colonic perforation.  Adult diapers have the disadvantage of keeping waste in contact with skin and can act as a barrier toevaporation of excess moisture if not change frequently.                                   TREATMENT        When Prevention fails, an aggressive approach to therapy iswarranted.      ln 1988, the National Pressure Sore Advisory Panel adopted Shea'spressure sore classification system (Figure 1-4) [4,27]. Treatment is guided by the five therapeutic principles outlined inTable 1 [28,29].      Improving the patient's general condition includes all the measures discussed under `Prevention'.  Elimination of all risk factorsis essential.     A complete nutritional assessment is advised. An adequate number of calories must be provided, either enterally or with venous hyperalimentation.  Several vitamins and minerals are important for wound healin#. Vitamin A is essential for epithelial maturation and collagen formations [30]. Vitamin C is needed for collaen synthesis, maintenance of connective tissue, and leukocyte function [31].  Folic acid is neyessary for protein synthesis and it enhances cell division [32].  Zinc is essential for protein synthesis and tissue repair# [33].All may be administered as oral supplements.      Some caution in the use of vitamin and mineral supplements is advised.  Serum zinc levels should be determined prior to starting supplements because excess zinc can interfere with wound healing. Additionally, zinc and folic acid bind to the same protein and must be given 12 hours apart. Doses are: Zinc sulfate, 220mg PO daily; Folicacid, lmg PO daily.      Vitamin A is of special concern.  It has been shown to counter the anti-inflammatory effects of steroids and stimulate wound healing. Toxicity can occur with doses in excess of 25,000 IU per day for several months [34,35,38].  I generally limit Vitamin A use to those patients who are steroid dependant and/or malnurished.  Vitamin A doseis 25,000 IU, p0 daily for 3-4 weeks.        ҁ   is an absolute!  All measures discussed under`PREVENTION' are applicable.  By their nature, Grade I and many small Grade II pressure sores will heal with relief ofpressure alone.        ΁ ΁ρ ΁Ӂԁ΁ÁŁ should the patient lie directly on an existing pressure sore.  If the patient cannot be turned frequently, or has large sacral, bilateral ischial, or trochanteric ulcers, the use of alow-air-loss or air fluidized bed should be considered.       The goal of   is to lower the bacterial count of the ulcer bed to less than 100,000 organisms/gram ulcer tissue. Bacterial counts higher than this will delay healing by interferingwith wound granulation [15,28,29].      The ideal disinfecting solution should not cause pain, change the character of the ulcer (e.g.:iodine staining), injure healthy tissue,or interfere with granulation tissue growth [29,36].      Most of the topical disinfectants in use today are toxic to fibroblasts and granulation tissue [37]. Their use  the wound is not recommended.  However, all are appropriate for skin cleansing   the margin of the wound.  Wound disinfection is accomplished by frequent irrigation, preferably under pressure (I use a waterpick), with sterilenormal saline, and a combination ofsharp and enzymatic debridement.      Because bacterial infection is usually limited to the ulceritself, cultures and antibiotics are rarely indicated.      Debridement is performed to remove necrotic tissue and eschar from the ulcer bed.  Both impeed healing and create an environment for bacterial proliferation.  The recommended approach is dailysharp debridement until all necrotic tissue is removed [15,29].  If daily sharp debridement cannot be done, proteolytic enzymes(desoxyribonuclease, fibrinolysin, or collagenase) may be used.      #equent dressing changes are also necessary. Gauze pads, moistened with sterile normal saline and wrung-out, are applied to the wound two or three times per day and allowed to dry. When the dressing is changed, necrotic tissue and debris that has adhered to the auze are removed with the dressing. This is an effective method of debridement, but can be painful.  Unfortunately, it also removes healthy granulation tissue with the debris.  Once the wound is clean, this method should bediscontinued.      Other techniques of debridement include irrigation under pressure and whirlpool baths.  Both work well but share the disadvanta#es of thewet-to-dry dressing technique.      Bedside debridement of large Grade 1II and IV ulcers may be ineffective.  In these cases, surgical debridement under anesthesia maybe necessary.      A favorable environment for granulation tissue formation exists only if the ulcer is clean, moist, free of necrotic debris, with abacterial count less than 100,000 organisms/gram tissue [38,39,40]. Hydrophilic, occlusive, gas permeable dressings are recommended for Grade II and small Grade III pressure sores.  Larger Grades III and IV ulcers are kept moist by packing the wound with normal saline or lactated ringer's moistened gauze that is kept moist between dressingchanges [29].        Large Grade III and IV ulcers may require surgical repair with skin grafts or myocutaneous flaps to replace skin and soft tissue losses.  Additionally, modification of the bony prominence underlyingthe ulcer may be necessary [41].      This author's method of pressure sore treatment, based on the available literature and personal experience, is also summarized inTable 1.                                  COMPLICATIONS        With few exceptions, routine wound cultures and systemic antibiotics are not indicated in the treatment of the uncomplicated pressure sore.  However, transient bacteremia can occur during debridement sessions and dressing changes.  In the immunosupressed patient, patients with a history of rheumatic heart disease, or in the presence of orthopedic, cardiac or vascular prosthesis, prophylacticantibiotics should be considered.      Most pressure sores are polymicrobial, consisting of common gram positive cocci and gram negative rods.  Without evidence of other sources of infection, the appearance of fever, chills, and leukocytosisindicates spread of infection beyond the pressure sore.      Cellulitis is an inflammation of the subcutaneous tissue around the pressure sore.  lt is characterized by swelling, redness, heat, and pain extending away from the wound margins.  A moderate to high fever and leukocytosis is usually present.  There can be accompaninglymphangitis [42,43].      Septicemia occurs when bacteria and their toxins are seeded directly into the bloodstream from an infected pressure sore. Septicemia is characterized by moderate to high fever, shaking chills. and an elevated white blood cell count.  There may be a relative bandemia on periPheral blood smear.  Septicemia is most frequently associated with multiple pressure sores.  Mortality in this group ofpatients approaches 50% [44,45].      If cellulitis or septicemia are suspected, wound and blood cultures for aerobes and anaerobes should be obtained.  Broad spectrum antibiotics that cover common gram positive and negative pathogens should be started. Antibiotic coverage can be tailored to the specificpathogen(s) once culture results are available.      Additional treatment for cellulitis includes elevation if an extremity is involved, hot packs, and wound debridement.  Failure to see improvement after 24 hours of appropriate treatment suggests the presence of an abscess or a resistant organism.  An abscess requires prompt surgical drainage [43]. The suspicion of a resistant organismrequires reconsideration of antibiotic coverage.      In cases of septicemia, prompt recognition and treatment is necessary to prevent frank sepsis.  Other supportive measures (hemodynamic monitoring, blood pressure support, etc) may also be necessary. If, on inspection, the pressure sores appear clean, othersources of sepsis should be considered.      Finally, because pressure ulcers occur in close proximity to bone, osteomyelitis must be considered when a pressure sore penetrates to or through periosteum, or if the ulcer fails to heal despite appropriate therapy. The diagnosis is often difficult to make, requiring a highindex of suspicion [46].         A number of studies looked at various radiologic aids to diagnosing osteomelitis [47,48].  They concluded that a normal Tc99m scan effectively ruled out osteomyelitis.  However, an abnormal scan indicated the need for further testing (i.e.; needle bone biopsy) to confirm the presence of osteomyelitis.  Plain radiographs proved usefulonly in pinpointing the best location for biopsy.                                 OTHER THERAPY        As our understanding of wound healing is increasing.  A variety of new, and not so new, technologies is being applied to pressure soretreatment with promising results.      Transcutaneous measurement of skin oxygen tension allows the direct measurement of the effects of pressure on skin perfusion[23]. Using the CO2 laser, the pressure sore can be excised, the ulcer bed sterilized, and the wound closed primarily with little risk ofinfection [49].      Research on the use of platelet derived epidermal growth factors, applied directly to the pressure sore or impregnated into dressings,has been shown to speed epithelialization [50].      Transcutaneous electrical stimulation of chronic pressure ulcershas also been shown to stimulate healing [51,52].                                   CONCLUSION        Pressure sores are an unfortunate problem that carries significant financial, emotional, and physical morbidity.  Using existing knowledge, tools, and techniques, "at-risk" patients can be identified and preventive measures taken.  An organized approach consistin# of acomprehensive, yet simple, prevention program is recommended.      Treatment of existing pressure sores can be time consuming and exasperating for patients, their families, and health care providers. By following the 5 therapeutic principles outlined here.  improvement and/or healing of these wounds will be facilitated.  Larger wounds necessitate the early involvement of a general or plastic surgeon withan interest in pressure sore management.                                                         BIBLIOGRAPHY         1.  Peterson NC, Bittmann S.  The epidemiology of pressure     sores.  Scand J Plast ReConstr Surg.  1971; 5:62-66.        2. Richardson RR, Meyer PR.  Prevalence and incidence of pressure     sores in acute spinal cord injuries.     Paraplegia 1981; 19:235-47.       3. Versluysen M. Pressure sores in elderly patients.     J. Bone Joint Surg. 1985, 87-B(1):10-13 British Edition.        4. The National Sore Advisory Panel.  pressure ulcer prevalence,      cost and risk assessment: consensus development conference     statement.  Decubitus 1989; 2(2):24-28       5. Shannon ML, Skorga P.  pressure ulcer prevalence in two     general hospitals.  Decubitus 1989;  2(4):38-43.       6. Allman #M, LaPrade CA, Noel LB, Walker JM, Moorer CA,     Dear M, Smith CR.  Pressure sores among hospitalized patients.     Ann Int Med 1986; 105:337-42       7. Hibbs P.  The economics of pressure ulcer prevention.     Decubitus 1988; 1(3):32-38.        8. Reuler JB, Cooney TG.  Pressure sores: when prevention fails.     Hosp Prac 1985; 20:14-24.        9. Landis EM.  Microinjection studies of capillary blood pressure     in human skin.  Heart 1930; 15:209-228.       10. Kosiak M, Kubicek WG, Olson M, Danz JN, Kottke, FJ.      Evaluation of pressure as a factor in the production of ischial     ulcers.  Arch Phys Med Rehabil. 1958; 39:623-30.       11. Kosiak M.  Etiology and pathology of ischemic ulcers.     Arch Phys Med Rehabil.  1959; 40:62-69        12. Nola GT, Vistnes LM.  Differential response of skin and muscle      in the experimental production of pressure sores.  Plast Reconstr     Surg.  1980; 66(5):728-35.       13. Daniel RK, Priest DL, Wheatlry DC.  Etiologic factors in     pressure sores: an experimental model.     Arch Phys Med Rehabil.  1981; 62:492-8.       14. Bennett L, Kavner D, Lee BK, Trainor FA.  Shear vs.      pressure as causative factors in skin blood flow occlusion.  Arch     Phys Med Rehabil.  1979; 60:309-14.      15. Longe RL  Current concepts in clinical therapeutics:     pressure sores.  Clin Pharm 1986; 5:669-81.       16. Levine LM, Simpson M, McDonald RJ.  Pressure sores: a     plan for primary care prevention.  Geriatrics 1989; 44(4):75-90.      17. Exton Smith AN, Sherwin RW.  The prevention of pressure     sores.  Significance of spontaneous body movements.     Lancet 1611; 2:1124-28.       18. Fenske NA, Conrad CB.  Aging skin.     Amer Fam Pract 1988; 37:211-30.       19. Bennett G.  Ageing skin and pressure sores.     The Practitioner 1987; 231:834-840.       20. Pinchcofsky-Devin GD, Kaminski MV.  Correlation of     pressure sores and nutritional status.     J Am Geriatr Soc 1986;  34:435-440.       21. Gosnell DJ.  An assessment tool to identify pressure     sores.  Nurs Res 1973; 22(1):55-62.       22. Norton D, McLaren R, Exton-Smith AN:            󁮁     Edinburgh, Churchill-Livingston, 1982, pp194-236.      23.  Seiler WO, Stahelin HB.  Decubitus ulcers: preventive     techniques for the elderly patient.     Geriatrics 1985; 40(7):53-60.      24. Wiley T.  High tech beds and mattress overlays.     Am J Nurs 1989;  89:1142-1145.       25. Bennett RG, Bellantoni MF, Ouslander JG.  Air-fluidized     bed treatment of nursing home patients with pressure sores.     J Am Geriatr Soc 1989; 37:235-242.       26. Clark M, Rowland LB.  Preventing pressure sores: matching      patient and mattress using interface pressure measurements.     Decubitus 1989; 2(1):34-39.      27. Shea JD.  Pressure sores: classification and management.     Clin Orthop 1975; 112:89-100.       28. Knight AL.  Medical management of pressure sores.     J Fam Pract 1988; 27:95-100.      29. Seiler WO, Stahelin HB.  Decubitus ulcers; treatment     through five therapeutic principles.     Geriatrics 1985; 40(8):30-44.       30. Olson JA.  Recommended dietary intakes of vitamin A in     humans.  Am J Clin Nutr 1986; 43:258-62       31.  Taylor TV, Rimmer #, Da# B, Butcher J, Dymock IW.      Ascorbic acid supplementation in the treatment of pressure sores.      Lancet 1974; 2:544-546.       32. Herbert V. Recommended dietary intakes of folate in     humans.  Am J Clin Nutr 1987; 45:661-70.       33. Liszewski RF .  The effect of zinc on wound healing: a     collective review.  J.A.O.A. 1981; 81:104-109.     34. Hunt TK, Ehrlich HP, Garcia JA, et al.  Effects of      vitamin a in reversing the inhibitory effects of cortisone on     healing of open wounds in animals and man.     Ann Surg 1969; 170:633-41       35. Hunt TK.  Vitamin A and wound healing.     J Am Acad Dermatol  1986; 15:817-821      36. Silverman AK, Ellis CN, Voorhees JJ.  Hypervitaminosis A     syndrome: a paradigm of retinoid side effects.     J Am Acad Dermatol  1987; 16:1027-1039      37. Lineaweaver W, Howard R, et al.  Topical antimicrobial     toxicity.  Arch Surg  1985; 120:267-270      38. Alper JC.  Recent advances in moist wound healing.     South Med J  1986; 79:1398-404      39. Gorse GJ, Messner RL.  Improved pressure sore healing     with hydrocolloid dressings.     Arch Dermatol  1987; 123:766-71      40. Oleske DM, Smith XP, White P, et al.  A randomized     clinical trial of two dressing methods for the treatment     of low-grade pressure sores.     J Enterost Ther  1986; 13:90-98      41. Vasconez LO, Schneider WJ, Jurkiewicz MJ. Pressure     sores.  Curr Probl Surg  1977; 14:1-62      42. Cohn I, Bormside GH.  Infection.  In Schwartz SI et al (ed):     Ё  Ӂ .  New York, McGraw-Hill, 1989      43.  Way LW (ed).  Á Ӂ ā  ԁ􁮁     Appleton & Lang, Norwalk, Connecticut, 1988      44. Galpin JE, Chow AW, Bayer AS, Guze LB.  Sepsis associated     with decubitus ulcers.  Am J Med  1976; 61:346-50      45. Bryan CS, Dew CE, Reynolds KL.  Bacteremia associated     with decubitus ulcers.  Arch Intern Med  1983; 143:2093-5       48. Dimant J, Tanael L. Decubitus ulcers:when to suspect     osteomyelitis.  Geriatrics  1987;  42:74-83.       47. Sugermann B.  Pressure sores and underlying bone     infection.  Arch Intern Med. 1987;  147:553-55.       48. Thornhill-Joynes M, Gonzales F, Stewart CA, Kanel GC,      Lee GC. Capen DA, et al.  Osteomyelitis associated with pressure     ulcers. Arch Phys Med Rehabil  1986; 67:314-18       49. Hinshaw JR, Herrera HR, Lanzafame RJ, Pennino RP.  The      use of the carbon dioxide laser permits primary closure of     contaminated and purulent lesions and wounds.     Lasers Surg Med 1987;  6:581-583        50. Knighton DR, Ciresi K, Fiegel VD, Schumerth S, Butler E,      Cerra F. Stimulation of repair in chronic, nonhealing, cutaneous     ulcers using platelet-derived wound healing formula.     Surg Gyn OB  1990; 170:56-60       51. Barron JJ, Jacobson WE, Tidd G. Treatment of decubitus     ulcers-a new approach.  Minn Med 198;  68:183-6       52. Kloth LC, Feedar JA.  Acceleration of wound healing with     high voltage, monophasic, pulsed current.     Phys Ther 1988;  88:503-8                FIGURE 1     Grade I:  Localized area of heat, induration, and erythema with an     irregular, ill defined border, usually over a bony prominence.     Epidermis is usually intact, but there may be a shallow ulcer    present [27].       FlGURE 2    Grade II:  All characteristics of Grade 1 but with an ulcer that    extends through epidermis down to but not into subcutaneous tissue.   May be tender to touch is sensation is intact [27].       FlGURE 3    Grade III:  Is a full-thickness wound extending to, but not through,    fascia.  Dermal undermining is present for varying distances from    the wound edge.  The sore is usually infected, foul smelling, with   a necrotic base.  An eschar may be present [27].       FIGURE 4    Grade IV:  Has all the characteristics of Grade 3 but penetrates    through fascia.  Muscle or bone may be visible in the ulcer base.   Dermal undermining is usually extensive {27}.             K 
#(-27<N 
#(-27<                                TABLE 1               APPROACHES TO TREATMENT OF PRESSURE SORES   Ё偠ǁ偠    Pressure    Foam or static air    Alternating air      Low air loss or  Relief      mattress overlay      pressure mattress    air-fluidized bed                                                        system            Turn q2h into 30 degree right and left lateral oblique   Shear       Head of bed flat/< 30 degrees Dis-        none                                       Clean to wound Infection                                             edges using 0.001%                                                       Providine-iodine                                                       solution Debridement none                                       Daily sharp removal                                                        of eschar,necrotic                                                        tissue, debris.                                                        Colagenase used                                                        Whirlpool qd-qod                                                        Normal saline wet-                                                        to-dry dressing                                                        changes q8h until                                                        wound clean Promote                           Hydrocolloid         Ringer's solution Granulation                       occlusive            wet dressing:keep                                   dressing             moist                                                         General/Plastic                                                        Surgery consult                                                        for definative                                                        repairN 
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